2. Zoonotic disease
Caused by the spirochete Leptospira
Historically known as Weil’s disease
Described in 1885 by Adolf Weil with clinical hallmarks of
splenomegaly
jaundice
nephritis
Introduction
3. One of the emerging infectious diseases since the late 1990s
Recent large outbreaks in several Asian, Central and South
American countries
Becoming an important public health problem, yet it
continues to be under recognized
4.
Genus Leptospira, order Spirochetales, family
leptospiraceae
Can live both in animals and free in the environment
(both pathogenic and saprophytic)
Around 250 serovars from 20 species cause disease in
humans and animals
Organism
5.
All species are morphologically identical
Tightly and regularly coiled with hooked ends
Highly motile along the longitudinal axis
Morphology
6.
7. Not seen by direct light microscopy
Dark-field or phase contrast microscopy must be used
In tissues
silver impregnation (Warthin starry staining),
immunohistochemistry or
immunoflourescence microscopy
Isolation difficult
8.
Zoonotic disease
No human to human transmission
Most important sources are rats, dogs, cattle and pigs
Epidemiology
9. Domestic animals : temporary carrier
Rodents : permanent carrier
Rodents are therefore considered as the major reservoir of
infection.
Rat (Rattus norvegicus and Rattus rattus) associated L.
interrogans serovars Icterohaemorrhagic and Copenhageni
are mostly associated with Weil’s disease
10. Transmitted through contact with infected animal urine
and other excreta (e.g. placenta)
Contact may be
direct or
indirect through surface water or moist soil
11.
12. Patterns of transmission can be
Epidemic
Endemic
Sporadic
13. Seasonal rains and flooding are the most important
factors causing epidemics
Endemic disease is facilitated by
Tropical humid environment
Poor sanitation
Rodent and dog population
14. • Sporadic disease is associated with
Occupation : veterinary, sewer and slaughterhouse
workers
Poor hygiene areas e.g. slums
Adventure travel
Military training
15. No precise estimates of the global burden of human
leptospirosis
Estimated annual incidence (WHO) – 0.1 to 1 per 100 000
per year in temperate climates – 10 or more per 100 000
per year in the humid tropics.
Estimated case-fatality rates in different parts of the
world have been reported to range from <5% - 30%
16. Figures are grossly underestimated : Overlooked and
under reported
Why the lack of recognition?
Clinical manifestation wide and varied
May mimic many other diseases, e.g. dengue fever and
other viral haemorrhagic diseases
Diagnostic capabilities are not readily available
(especially in endemic countries)
Poor surveillance and reporting of cases
17.
Considered a rare zoonotic disease in India with only
sporadic cases being recorded.
Since 1980’s the disease has been reported from various
states during monsoon months in mini epidemic
proportions.
Indian perspective
18. In India, urban leptospirosis has been reported from
Chennai & Mumbai while rural leptospirosis has been
reported from Gujarat, Kerala and Andamans
Non-reporting of leptospirosis from other states of India
does not mean that it is absent in those parts.
19. The disease is endemic in
Kerala
Tamil nadu
Gujarat
Andamans
Karnataka
Maharashtra
It has also been reported from Andhra Pradesh, Orissa,
West Bengal, Uttar Pradesh, Delhi & Puducherry
20.
21. Leptospirosis has been under-reported and under-
diagnosed from India due to
lack of awareness of the disease and
lack of appropriate laboratory diagnostic facilities in most
parts of the country
22.
Organism disappears from blood but remains in
organs including brain , liver, lung, heart and
kidneys
Development of antibodies(5-7 days)
Proliferate in bloodstream and disseminate
hematogenously
Infects through mucosa ( conjunctival , oral) or
through punctured or abraded skin
Pathogenesis
23. Excreted in urine
Adhere to proximal tubule epithelial cells
Penetrate basement membrane of PCT
Traverse interstitial spaces of kidney
24. Hypovolaemic shock and vascular collapse
Loss of fluids into the third space
Vasculitis and leakage : petechiae , intra parenchymal
bleeding and bleeding along serosa and mucosa
Capillary vasculitis (endothelial necrosis and lymphocytic
infiltration)
Attach onto the endothelial cells
Produces endotoxin
25.
Clinical expression can be
Subclinical infection
Undifferentiated febrile illness
Weil’s disease
Incubation period 2-30 days (average 5-14 days)
Clinical features
26. Classically described as biphasic
Acute phase:
3-10 days
leptospiraemia : blood culture may be positive
fever responds to antibiotics
Immune phase :
fever does not respond to antibiotics
isolation from urine
27.
Conjunctival suffusion
Jaundice
Pharyngeal erythema without exudate
Rashes (maculopapular, erythematous, petechial or
ecchymotic)
Muscle tenderness
Rales in lungs
Meningismus
Hyporeflexia or areflexia
Physical examination
28.
29.
30.
The most severe form of leptospirosis
Monophasic and fulminant
Variable combinations of jaundice, acute kidney injury,
hypotension and hemorrhage
Pulmonary hemorrhage is the most common
Multisystem involvement occurs
Weil’s disease
31.
Presents with jaundice
Not associated with fulminant hepatic necrosis or liver
cell damage
LFTs are abnormal (<5 times the upper limit)
Liver can be enlarged and tender
Splenomegaly in a minority of patients
Liver involvement
32.
Can manifest after several days of illness
Can be oliguric/nonoliguric
Dyselectrolytemia is common: hypokalemia and
hypomagnesemia in nonoliguric disease
Hypotension may cause tubular necrosis and oliguria
May require vasopressor support and hemodialysis
Kidney involvement
33.
Manifests with cough,
chest pain and hemoptysis
Purulent sputum
uncommon
Severe pulmonary
hemorrhage occurs in endemic disease
Alveolar infiltrates are visible on CXR
Pulmonary involvement
34. Cardiac :
Myocarditis
Neurological :
Aseptic meningitis
Hypo or areflexia
Eyes :
Uveitis
Skeletal muscles :
Severe myalgia of calves and abdominal muscles
Cholecystitis
Pancreatitis (can cause hypo/hyperglycemia)
Other manifestations
35.
High index of suspicion is critical in a setting of
An appropriate exposure history
Infection’s protean manifestations
Biochemical, hematological and urinalysis may suggest
but are not specific for diagnosis
Diagnosis
36. The disease is usually diagnosed by –
detecting antibodies using various serological tests
culturing the bacteria from blood, urine or tissues
demonstrating the presence of leptospires in tissues using
antibodies labelled with fluorescent markers
polymerase chain reaction (PCR)
Immunostaining
Cultures take many weeks and cannot guide clinical care
Dark-field microscopy of blood/urine not recommended
39.
Microscopic agglutination test (MAT) is the gold
standard : Sensitivity 92% Specificity 95%
MAT has a very limited availability
Serological tests
40. The MAT entails growth of a battery of serovars
representing the 26 leptospiral serogroups , incubation of a
standard quantity of leptospires with the patient’s serum
on a microtiter plate, and detection of agglutination by
dark-field microscopy.
The highest dilution of serum that yields significant (50%)
agglutination is reported as the titer.
41. When patients have a high pretest probability: a single
antibody titer >1:200 is considered strong evidence of
infection
In regions where leptospirosis transmission and subclinical
disease are common, higher titers are generally required
MAT is generally negative in the first 7–10 days after the
onset of infection
Paired acute- and convalescent-phase serum samples are
preferred to document seroconversion or a fourfold rise in
titer.
43. Genus specific or rapid tests include
ELISA
Macroscopic slide agglutination test (MSAT)
Latex agglutination test
Dipstick tests ( Lepto dipstick, Lepto Tek lateral flow)
Lepto Tek Dri-Dot test
Indirect hemagglutination
44. These tests are simple, more sensitive and become
positive earlier than MAT (5-6th day) as they detect
specific IgM antibodies
Use saphrophytic leptospira as antigens
Are commercially available
45.
Leptospires can be cultured from blood and CSF
during first 7-10 days
Urine culture useful beginning in the 2nd week
May take 2-4 weeks to be positive
Urine cultures can remain positive for many
months/years despite therapy
Isolation
51.
Prompt initiation of antibiotic therapy shortens the
course and prevents progression
Mild leptospirosis resolves without any treatment
Treatment
52.
53. Renal involvement may require hemodialysis
Hypotension can be managed by fluids and vasopressors
Severe disease should be treated empirically with broad-
spectrum antibiotics before confirmation
54.
Advanced age, pulmonary involvement, elevated
creatinine , oliguria and thrombocytopenia indicate poor
prognosis
Liver dysfunction has not been confirmed to be an
independent risk factor for death
No permanent sequelae or progressive organ
dysfunction after resolution
Prognosis
55. No vaccine available currently
Short-term antibiotic prophylaxis can be used for well-
defined exposures
Doxycycline 100 mg or Azithromycin 250mg once a week
may be used
Long-term antibiotic prophylaxis ineffective
General sanitation measures and avoidance of swimming in
contaminated places
Prevention
56.
Adequate history of exposure is most important in
diagnosis
Possibility of leptospirosis to be kept in d/d of all icteric
illness
Prompt treatment can prevent life threatening
complications
Health education and awareness for prevention
Take Home Message
